Kerry McDonald, Ph.D.
Research Interests
My research focuses on the cellular and
molecular mechanisms involved in the
regulation of striated muscle contraction
and how these regulatory processes are
altered by disease and other physiological
stresses such as exercise. To address these
questions, my lab takes a multi-faceted
approach incorporating tissue, cellular, and
molecular preparations. For many of our experiments,we utilize preparations of single
skeletal muscle fibers or single cardiac myocytes
from which the sarcolemma has been chemically removed while the myofilaments remain intact so that mechanical measurements can be made.
In these preparations the chemical environment surrounding the myofilaments can be
manipulated, allowing precise control of the cell's level of activation. Another advantage
of these preparations is that the protein composition from these cells can be experimentally
manipulated as well as quantified after mechanical measurements. Currently, my laboratory
is investigating the factors that regulate power output capacity of single cardiac myocytes,
which is a physiological variable that is essential for the heart to move blood throughout the
circulatory system. We are currently examining how power output is regulated by factors
such as contractile protein isoforms, activator calcium, sarcomere length, and phosphorylation
states of myofibrillar proteins. My research program also provides a means for trainees in our department to examine either the mechanical behavior or altered biochemical properties of striated muscle in response to
various models of muscle disease or altered muscle activity. For example, we currently are
collaborating with Dr. Harold Laughlin to examine whether cardiac muscle regulatory proteins, phosphorylation states of these proteins, and contractile properties of cardiac
myocytes are altered in response to exercise. We are also collaborating with Dr. Joe
Kornegay and Dr. Casey Childers in studies that examine mechanical changes of skeletal muscle in
response to a canine model of Duchenne's muscular dystrophy.
Professional Background
- B.A. in biology, Benedictine College, Received Ph.D. in biology, Marquette University
- NIH sponsored postdoctoral fellow, University of Wisconsin
- Joined Department in 1997
- Member of The Biophysical Society and The American Physiological Society
- Reviewer for several physiological journals
- Research currently funded by NIH and AHA
- Winner of the 2001 Dorsett L. Spurgeon M.D. Distinguished Medical Research Award, 2001
- NIG Independent Scientist Award (2003-2004)
Selected Publications
- Korte, F.S., E. Mokelke, M. Sturek and K.S. McDonald. Endurance exercise training enhances left ventricular function in diabetic dyslipidemic pigs: correlation with changes in cardiac myofibrillar proteins. J Appl Physiol (in press).
- Hinken, A.C. and K.S. McDonald. Inorganic phosphate speeds loaded shortening in skinned cardiac myocytes. Am. J. Physiol. 287:C500-C507, 2004.
- Childers, M.K. and K.S. McDonald. Skletal muscle fiber force and power increase with regulatory light chain phosphorlation. Muscle & Nerve. 29:313-317, 2004.
- Korte, F.S., K.S. McDonald, S.P. Harris, and R.L. Moss. Loaded shortening, power output and rate of force redevelopment are increased with knockout of cardiac myosin binding protein-C. Circ. Res. 93:752-758, 2003.
- McDonald, K.S. and T.J. Herron. It takes "heart" to win: What makes the heart powerful? New Physiol. Sci. 17:185-190, 2002.
- Herron, T.J. and K.S. McDonald. Small amounts of alpha-myosin heavy chain isoform
expression significantly increase power output of rat cardiac myocytes fragments. Circ. Res. 90:1150-1152, 2002.
- Herron, T.J., F.S. Korte and K.S. McDonald. Power output is increased following phosphorylation of myofibrillar proteins in skinned rat cardiac myocytes. Circ. Res. 89:1184-1190, 2001.
- McDonald, K.S. Ca2+ dependence of loaded shortening in rat skinned cardiac myocytes and skeletal muscle fibres. J. Physiol. (Lond.) 525:169-181, 2000.
Methodology/Techniques
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